Mineralogy of a Mudstone at Yellowknife Bay, Gale Crater, Mars

Sedimentary rocks at Yellowknife Bay (Gale Crater) on Mars include mudstone sampled by the Curiosity rover. The samples, John Klein and Cumberland, contain detrital basaltic minerals, Ca-sulfates, Fe oxide/hydroxides, Fe-sulfides, amorphous material, and trioctahedral smectites. The John Klein smectite has basal spacing of ~10 Å indicating little interlayer hydration. The Cumberland smectite has basal spacing at ~13.2 Å as well as ~10 Å. The ~13.2 Å spacing suggests a partially chloritized interlayer or interlayer Mg or Ca facilitating H_2O retention. Basaltic minerals in the mudstone are similar to those in nearby eolian deposits. However, the mudstone has far less Fe-forsterite, possibly lost with formation of smectite plus magnetite. Late Noachian/Early Hesperian or younger age indicates that clay mineral formation on Mars extended beyond Noachian time

Cytotoxic T cells are induced in mice infected with lymphocytic choriomeningitis virus strains of markedly different pathogenicities.

The ability of two lymphocytic choriomeningitis virus substrains to induce cytotoxic T-lymphocyte (CTL) responses in intracerebrally infected mice was examined. One strain, designated A (aggressive), provoked a convulsive type of death in 100% of the mice within 8 to 9 days, whereas the other strain, designated D (docile), killed less than 10% of the mice during 28-day observation periods. CTL activity was assessed by the capacity of partially purified splenocytes to lyse 51Cr-labeled L-cell targets infected with either type of lymphocytic choriomeningitis substrain. The CTL population was identified by its sensitivity to anti-Thy-1 serum and its inability to lyse uninfected target cells or infected target cells with which it differed at the level of antigens controlled by the major histocompatibility gene complex. A strong CTL response developed in mice infected with either lymphocytic choriomeningitis substrain, although the activity provoked by substrain D was somewhat less than that seen after substrain A infection. Peak CTL activities induced by both strains occurred at about the same time. Even though docile virus replicated more extensively in the brain than did aggressive virus and fluorescent antibody staining revealed similar distributions of viral antigen, no inflammatory response was noted in the brains of mice infected with docile virus. These results are discussed with regard to the role of CTLs in mediating classic central nervous system pathology

Lymphocytic choriomeningitis virus killer T cells are lethal only in weakly disseminated murine infections

The symptoms and histopathology of many virus diseases depend not so much on damage to cells by virus but on the immunobiological reaction to the infection. Nowhere is this more clearly illustrated than with murine lymphocytic choriomeningitis (LCM) 1 virus (1). The basic features of the system were established by Traub in the 1930's (2): mice that received virus transplacentally or shortly after birth developed a life-long peristent infection, whereas the outcome in mice infected as adults was quite different. In the latter case peripheral injection usually produced an abortive immunizing infection, whereas intracerebral (i.c.) injection resulted in choriomeningitis and death within 7-9 d. The immunological basis for this choriomeningitis has been investigated intensely during the last 10 yr. The early observations of Rowe (3) showing lack of correlation between serum antibody level and immunity, followed by the finding that thymectomized mice could not be killed by i.c. infection (4), were the first indications of the central role of thymus-derived lymphocytes in fatal lymphocytic choriomeningitis. Following the pioneering work of Volkert (5), Gilden et al. (6) established a mode